Biological explanations Flashcards
Research support- surface of the brain
- Cheng -> differences in thickness and size of surface of the brain (cerebral cortex, constructed of grey matter) could be the answer to the search for a reliable biomarker that could contribute to better diagnosis and treatment.
Dopamine hypothesis- neurotransmitters
Brain’s chemical messengers that appear to function differently in a person with schizophrenia. Dopamine is believed to be primarily involved- it is important in the functioning of multiple brain systems and can have implications for the symptoms of schizophrenia.
Hyperdopaminergia -> subcortex, high dopamine activity. Excess of dopamine receptors in Broca’s area associated with poverty of speech/ auditory hallucinations.
Hypodopaminergia -> cortex, abnormal dopamine systems. Goldman-Rakic et al (2004) identified a role for low levels of dopamine in prefrontal cortex in negative symptoms.
Genetic evidence
Gottesman (1991)
Showed the relationship between relatives and schizophrenia risk (%)
Conclusions: as genetic similarity increases, the risk of sharing schizophrenia increases. However, identical (MZ) twins share the same genetic material, so the fact that the risk is not 100% could indicate other factors are involved.
1st degree: Identical twins = 48%
Parents = 6%
2nd degree: Half siblings = 6%
Uncles/ Aunts = 2%
3rd degree: First cousins = 2%
General population = 1%
Candidate genes
- schizophrenia is said to be polygenic
- different combinations of factors can lead to schizophrenia- aetiologically heterogeneous.
- Ripke et al (2014)- conducted a meta analysis using genome-wide studies of schizophrenia.
- N=37,000 (Sz), N=113,000 (controls)
- 108 separate genetic variations associated with increased Sz risk.
Neural correlates
- measurements of the structure or function of the brain that correlate with schizophrenia.
- both positive and negative symptoms have neural correlates.
Neural correlates for positive symptoms
- Broca’s area: responsible for speech production and the muscle movement to speak. Reduced information flow in schizophrenics coincides with auditory hallucinations. The synchronisation of Broca and Wernicke’s area is reduced producing an effect on emotional speech activity.
- Cingulate gyrus: regulates emotional responses and social behaviour, as well as being involved in attention, memory, and perception. Lower activation levels in the anterior cingulate gyrus contribute to hallucinations. Allen et al (2007) investigated this through comparison to a control group, in determining whether recorded voices were their own or others.
- Temporal gyrus:
Neural correlates for negative symptoms
- Basal ganglia- responsible for motor movements (voluntary movements), emotions, habit formation, reward, and addiction. Patients with schizophrenia show a decrease in basal ganglia activity, leading habits and rewards to remain unsubstantiated, potentially contributing to avolition.
- Auditory cortex in temporal lobe- processes and interprets sounds. Analyses and decodes auditory information. Early auditory processing deficit, contributes to cognitive impairments.
- ventral striatum:
AO3: correlation- causation problem
- number of neural correlates of Sz symptoms, both positive and negative. Studies that focus on the role of brain systems in Sz leave questions about other explanations for this correlation.
- correlation between levels of activity in the ventral striatum and negative symptoms of Sz. It is possible that negative symptoms means less info passes through the striatum, resulting in reduced activity.
- existence of neural correlates could tell us little about Sz
AO3: evidence
- evidence for genetic vulnerability.
- Gottesman (1991)- genetic similarity and shared risk are related.
- Tienari (2004) adoption studies showed biological children of schizophrenic parents have a heightened risk- even if adopted.
- Hilker (2018)- concordance rate of 33% for identical twins and 7% for non-identical twins
- genetics make people vulnerable.
AO3: Mutation
- alternative theory supports genetic explanation.
- mutation- parental DNA/ paternal sperm cells- radiation or viral infections.
- Brown et al (2002)- positive correlation between paternal age and risk of schizophrenia increasing from 0.7%- fathers under 25 and 2% in fathers over 50.
- genetic factors in development of schizophrenia.
AO3: Mixed evidence
- for dopamine hypothesis
- dopamine agonists (amphetamines) increase levels of dopamine, which can make Sz worse and produce Sz like symptoms in some individuals- Curran 2004.
